Component

Vascular endothelial growth factor A

Vascular endothelial growth factor A. Species, exposure and limitations are retained in each linked claim.

4 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

How nutrients influence it

Every nutrient with a recorded effect on this component, credited to the nutrient that acted rather than the chapter that recorded it. Open a nutrient to see the findings and the conditions they were measured under.

How nutrients reach it in more than one step

Chains of two or more recorded steps that end here, grouped by the nutrient they start from. Each step is a separate finding, so a chain is a route a mechanism could take, not proof that it does.

Tracing routes…

What it does

Every recorded relationship this component is part of, grouped by its role. Plain wording comes first; the technical statement follows.

Recorded relationships

What acts on it

  1. Treatment significantly increased nitrate, VEGF and basic fibroblast growth factor levels and stabilised HIF-1alpha within one day, promoting blood vessel formation at 3 to 7 days and muscle healing at 5 to 7 days after contusion.

    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/hbot-research/32066777.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f8915aa50d5b22722e66d20eb0542c6bb03b76a3182d37215a53bc9238ac697d", "start_char": 0, "end_char": 1357, "text_sha256": "f8915aa50d5b22722e66d20eb0542c6bb03b76a3182d37215a53bc9238ac697d"}
    experimental_model
    Contused rat skeletal muscle with a reactive oxygen species scavenger and a nitric oxide synthase inhibitor
    exposure
    2.5 ATA 100% oxygen for 120 minutes daily for 5 consecutive days
    limitations
    Both inhibitors were given before treatment, which is what makes the requirement claim interpretable. The exposure is a therapy-like protocol, unlike the extreme-pressure studies recorded elsewhere here.
    nutrient_topic
    Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. · Hyperbaric oxygen therapy
    organism
    Rat
    plain_language
    Within a day the growth signals rise; within a week there are new vessels and repaired muscle.
    primary_references
    [hbot-p32066777] VEGF and bFGF induction by nitric oxide is associated with hyperbaric oxygen-induced angiogenesis and muscle regeneration. (2020). https://pubmed.ncbi.nlm.nih.gov/32066777/ DOI: 10.1038/s41598-020-59615-x
    tissue_or_cell_type
    Skeletal muscle

    Hyperbaric oxygen: the exposure, its reactive species, the signals they carry, and the nutrient-dependent enzymes that handle them (2026-09-19) · lines 686–697

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Contused rat skeletal muscle with a reactive oxygen species scavenger and a nitric oxide synthase inhibitor · source_derived_draft · unverified_draft

    ### hbot-no-vegf-bfgf Treatment significantly increased nitrate, VEGF and basic fibroblast growth factor levels and stabilised HIF-1alpha within one day, promoting blood vessel formation at 3 to 7 days and muscle healing at 5 to 7 days after contusion. Condition category: normal nutrient_topic: Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. plain_language: Within a day the growth signals rise; within a week there are new vessels and repaired muscle. organism: Rat tissue_or_cell_type: Skeletal muscle experimental_model: Contused rat skeletal muscle with a reactive oxygen species scavenger and a nitric oxide synthase inhibitor limitations: Both inhibitors were given before treatment, which is what makes the requirement claim interpretable. The exposure is a therapy-like protocol, unlike the extreme-pressure studies recorded elsewhere here. exposure: 2.5 ATA 100% oxygen for 120 minutes daily for 5 consecutive days evidence_span: {"source_cache": "artifacts/hbot-research/32066777.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f8915aa50d5b22722e66d20eb0542c6bb03b76a3182d37215a53bc9238ac697d", "start_char": 0, "end_char": 1357, "text_sha256": "f8915aa50d5b22722e66d20eb0542c6bb03b76a3182d37215a53bc9238ac697d"} [hbot-p32066777] VEGF and bFGF induction by nitric oxide is associated with hyperbaric oxygen-induced angiogenesis and muscle regeneration. (2020). https://pubmed.ncbi.nlm.nih.gov/32066777/ DOI: 10.1038/s41598-020-59615-x
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Treatment increased tissue levels of the angiogenesis markers EGF, VEGF, PDGF, FGF-2 and CXCL10, and Nrf2 correlated positively with EGF, VEGF and PDGF.

    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/hbot-research/31035003.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e0b19a857412f1a255ecc82052eb403389bcf5596a562828c04558e1d4354efc", "start_char": 0, "end_char": 1966, "text_sha256": "e0b19a857412f1a255ecc82052eb403389bcf5596a562828c04558e1d4354efc"}
    experimental_model
    Randomised comparison of 32 patients receiving standard wound care with or without hyperbaric oxygen, with ulcer tissue biopsies
    exposure
    Hyperbaric oxygen with standard wound care for 20 days
    limitations
    A small randomised human study with tissue-level molecular endpoints. Correlations between Nrf2 and growth factors are associations within treated tissue.
    nutrient_topic
    Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. · Hyperbaric oxygen therapy
    organism
    Human
    plain_language
    Five different growth signals rose together in the treated wound.
    primary_references
    [hbot-p31035003] Tissue-specific role of Nrf2 in the treatment of diabetic foot ulcers during hyperbaric oxygen therapy. (2019). https://pubmed.ncbi.nlm.nih.gov/31035003/ DOI: 10.1016/j.freeradbiomed.2019.04.031
    tissue_or_cell_type
    Diabetic foot ulcer tissue

    Hyperbaric oxygen: the exposure, its reactive species, the signals they carry, and the nutrient-dependent enzymes that handle them (2026-09-19) · lines 829–840

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomised comparison of 32 patients receiving standard wound care with or without hyperbaric oxygen, with ulcer tissue biopsies · source_derived_draft · unverified_draft

    ### hbot-angiogenic-markers Treatment increased tissue levels of the angiogenesis markers EGF, VEGF, PDGF, FGF-2 and CXCL10, and Nrf2 correlated positively with EGF, VEGF and PDGF. Condition category: normal nutrient_topic: Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. plain_language: Five different growth signals rose together in the treated wound. organism: Human tissue_or_cell_type: Diabetic foot ulcer tissue experimental_model: Randomised comparison of 32 patients receiving standard wound care with or without hyperbaric oxygen, with ulcer tissue biopsies limitations: A small randomised human study with tissue-level molecular endpoints. Correlations between Nrf2 and growth factors are associations within treated tissue. exposure: Hyperbaric oxygen with standard wound care for 20 days evidence_span: {"source_cache": "artifacts/hbot-research/31035003.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e0b19a857412f1a255ecc82052eb403389bcf5596a562828c04558e1d4354efc", "start_char": 0, "end_char": 1966, "text_sha256": "e0b19a857412f1a255ecc82052eb403389bcf5596a562828c04558e1d4354efc"} [hbot-p31035003] Tissue-specific role of Nrf2 in the treatment of diabetic foot ulcers during hyperbaric oxygen therapy. (2019). https://pubmed.ncbi.nlm.nih.gov/31035003/ DOI: 10.1016/j.freeradbiomed.2019.04.031
    Complete structured claim and evidence
  2. Treatment promoted expression of HIF-1alpha, NF-kappaB, VEGFA, SDF-1, VEGFR2 and CXCR4, with SDF-1 and VEGFA rising in human skin fibroblasts and CXCR4 and VEGFR2 rising in endothelial cells.

    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/hbot-research/32791151.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "106ed876131af9161051c4c178d88af4afd707a20e56a91447d35aa9ed290188", "start_char": 0, "end_char": 1662, "text_sha256": "106ed876131af9161051c4c178d88af4afd707a20e56a91447d35aa9ed290188"}
    experimental_model
    Diabetic foot mouse model with human skin fibroblasts and human umbilical vein endothelial cells
    exposure
    Hyperbaric oxygen with high glucose in vitro
    limitations
    Cell and mouse work with expression endpoints. Tube formation is an angiogenesis surrogate, not a vessel in a person.
    nutrient_topic
    Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. · Hyperbaric oxygen therapy
    organism
    Mouse and human cells
    plain_language
    The signal and its receptor go up on two different cell types at once, which is what lets them find each other.
    primary_references
    [hbot-p32791151] Hyperbaric oxygen potentiates diabetic wound healing by promoting fibroblast cell proliferation and endothelial cell angiogenesis. (2020). https://pubmed.ncbi.nlm.nih.gov/32791151/ DOI: 10.1016/j.lfs.2020.118246
    tissue_or_cell_type
    Skin wound, fibroblasts and endothelium

    Hyperbaric oxygen: the exposure, its reactive species, the signals they carry, and the nutrient-dependent enzymes that handle them (2026-09-19) · lines 660–671

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Diabetic foot mouse model with human skin fibroblasts and human umbilical vein endothelial cells · source_derived_draft · unverified_draft

    ### hbot-hif-vegf-sdf-axis Treatment promoted expression of HIF-1alpha, NF-kappaB, VEGFA, SDF-1, VEGFR2 and CXCR4, with SDF-1 and VEGFA rising in human skin fibroblasts and CXCR4 and VEGFR2 rising in endothelial cells. Condition category: normal nutrient_topic: Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. plain_language: The signal and its receptor go up on two different cell types at once, which is what lets them find each other. organism: Mouse and human cells tissue_or_cell_type: Skin wound, fibroblasts and endothelium experimental_model: Diabetic foot mouse model with human skin fibroblasts and human umbilical vein endothelial cells limitations: Cell and mouse work with expression endpoints. Tube formation is an angiogenesis surrogate, not a vessel in a person. exposure: Hyperbaric oxygen with high glucose in vitro evidence_span: {"source_cache": "artifacts/hbot-research/32791151.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "106ed876131af9161051c4c178d88af4afd707a20e56a91447d35aa9ed290188", "start_char": 0, "end_char": 1662, "text_sha256": "106ed876131af9161051c4c178d88af4afd707a20e56a91447d35aa9ed290188"} [hbot-p32791151] Hyperbaric oxygen potentiates diabetic wound healing by promoting fibroblast cell proliferation and endothelial cell angiogenesis. (2020). https://pubmed.ncbi.nlm.nih.gov/32791151/ DOI: 10.1016/j.lfs.2020.118246
    Complete structured claim and evidence
  3. Dihydrocapsaicin at 10 mg/kg increased the expression of hypoxia inducible factor 1 alpha, vascular endothelial growth factor and matrix metalloprotease 9 at 3 and 14 days after ischaemia-reperfusion and of angiopoietin 1 and its receptor Tie-2 at 14 days, with angiogenesis confirmed by BrdU labelling co-localised with von Willebrand factor, alongside decreased neurological deficit scores and infarct volume and improved rotarod and pole test performance.

    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/dihydrocapsaicin-research/32107104.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a00c09c7443e15a674b7e9c6451ddd60a161f69ff98e33c32bcce0039662f8b1", "start_char": 0, "end_char": 1350, "text_sha256": "a00c09c7443e15a674b7e9c6451ddd60a161f69ff98e33c32bcce0039662f8b1"}
    experimental_model
    Fourteen-day outcome study after middle cerebral artery occlusion in rats with BrdU labelling
    exposure
    Dihydrocapsaicin at 10 mg/kg body weight after 2 hours of occlusion
    limitations
    The dose here is roughly an order of magnitude above the hypothermia studies and no temperature is reported, so this may not be a hypothermic effect at all. Recorded with that stated.
    nutrient_topic
    Dihydrocapsaicin research collection; topical membership is not evidence of a direct clinical effect, and dihydrocapsaicin is recorded separately from capsaicin. · Dihydrocapsaicin
    organism
    Rat
    plain_language
    At a much larger dose it made new blood vessels grow into the damaged area over two weeks.
    primary_references
    [dhc-p32107104] Dihydrocapsaicin-induced angiogenesis and improved functional recovery after cerebral ischemia and reperfusion in a rat model. (2020). https://pubmed.ncbi.nlm.nih.gov/32107104/ DOI: 10.1016/j.jphs.2020.02.001
    tissue_or_cell_type
    Brain vasculature

    Dihydrocapsaicin: the second capsaicinoid, the hypothermia it is used to induce, what the gut and liver do to it, and what it does without TRPV1 (2026-09-21) · lines 465–476

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Fourteen-day outcome study after middle cerebral artery occlusion in rats with BrdU labelling · source_derived_draft · unverified_draft

    ### dhc-angiogenesis-at-high-dose Dihydrocapsaicin at 10 mg/kg increased the expression of hypoxia inducible factor 1 alpha, vascular endothelial growth factor and matrix metalloprotease 9 at 3 and 14 days after ischaemia-reperfusion and of angiopoietin 1 and its receptor Tie-2 at 14 days, with angiogenesis confirmed by BrdU labelling co-localised with von Willebrand factor, alongside decreased neurological deficit scores and infarct volume and improved rotarod and pole test performance. Condition category: normal nutrient_topic: Dihydrocapsaicin research collection; topical membership is not evidence of a direct clinical effect, and dihydrocapsaicin is recorded separately from capsaicin. plain_language: At a much larger dose it made new blood vessels grow into the damaged area over two weeks. organism: Rat tissue_or_cell_type: Brain vasculature experimental_model: Fourteen-day outcome study after middle cerebral artery occlusion in rats with BrdU labelling limitations: The dose here is roughly an order of magnitude above the hypothermia studies and no temperature is reported, so this may not be a hypothermic effect at all. Recorded with that stated. exposure: Dihydrocapsaicin at 10 mg/kg body weight after 2 hours of occlusion evidence_span: {"source_cache": "artifacts/dihydrocapsaicin-research/32107104.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a00c09c7443e15a674b7e9c6451ddd60a161f69ff98e33c32bcce0039662f8b1", "start_char": 0, "end_char": 1350, "text_sha256": "a00c09c7443e15a674b7e9c6451ddd60a161f69ff98e33c32bcce0039662f8b1"} [dhc-p32107104] Dihydrocapsaicin-induced angiogenesis and improved functional recovery after cerebral ischemia and reperfusion in a rat model. (2020). https://pubmed.ncbi.nlm.nih.gov/32107104/ DOI: 10.1016/j.jphs.2020.02.001
    Complete structured claim and evidence

In the sources

Preserved passages that mention this component, quoted exactly. Open one to read it in context.

    This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.

    Evidence, AI assistance and curation standards